# Tamarixetin: A Promising Bioflavonoid Against Acetaminophen-Induced Liver Injury

**Authors:** Mehmet Ali Telafarlı, Ejder Saylav Bora, Firdes Topal, Oytun Erbaş

PMC · DOI: 10.3390/cimb47070524 · 2025-07-08

## TL;DR

Tamarixetin, a natural flavonoid, shows promise in protecting the liver from acetaminophen overdose by reducing oxidative stress and inflammation.

## Contribution

This study is the first to investigate tamarixetin's protective effects against acetaminophen-induced liver injury in a rat model.

## Key findings

- Tamarixetin significantly reduced liver damage markers like ALT and MDA in rats with acetaminophen-induced injury.
- Tamarixetin restored antioxidant levels and improved histopathological outcomes in the liver.
- Tamarixetin increased HSP-70 expression, indicating modulation of the stress response.

## Abstract

Oxidative stress, mitochondrial dysfunction, and inflammatory responses cause acute liver failure in most cases of acetaminophen (APAP) overdose. Tamarixetin (Trx), an antioxidant and anti-inflammatory flavonoid, has not yet been studied in models of APAP-induced hepatotoxicity. Trx was tested for its protective effects on APAP-induced liver injury in rats using biochemical, histopathological, and oxidative stress parameters. Three groups of 30 male Wistar rats were randomly assigned to the following groups: control, APAP + Saline, and APAP + Trx (3 mg/kg/day, intraperitoneally for 3 days). A single 300 mg/kg intraperitoneal APAP dose caused hepatotoxicity. ALT, MDA, GSH, HSP-70, and thioredoxin were measured in blood and liver tissues. Liver sections were histopathologically examined. APAP depleted hepatic GSH and Trx and increased serum ALT and MDA. Trx treatment significantly reduced ALT (201.2 → 105.1 U/L), MDA (5.5 → 3.4 nmol/mg), and the percentage of histologically damaged hepatocytes (58.5% → 9.5%), while restoring GSH and thioredoxin levels. Notably, HSP-70 expression exceeded that of APAP and control levels, suggesting the modulation of the stress response. The Trx group showed significant hepatoprotection histologically. Trx reduces APAP-induced hepatic damage, likely through antioxidant and anti-inflammatory mechanisms. These findings suggest that Trx may be a natural hepatoprotectant, warranting clinical trials.

## Linked entities

- **Proteins:** HSPA1A (heat shock protein family A (Hsp70) member 1A), TRX1 (thioredoxin H-type 1)
- **Chemicals:** acetaminophen (PubChem CID 1983), Tamarixetin (PubChem CID 5281699), ALT (PubChem CID 10219674), MDA (PubChem CID 1614), GSH (PubChem CID 124886)

## Full-text entities

- **Genes:** Txn1 (thioredoxin 1) [NCBI Gene 116484] {aka Txn}, Hspa1b (heat shock protein family A (Hsp70) member 1B) [NCBI Gene 108348108] {aka HSP70, HSP70-1, HSP70.1, HSP70.2, Hsp70-2, Hsp72}
- **Diseases:** mitochondrial dysfunction (MESH:D028361), acute liver failure (MESH:D017114), overdose (MESH:D062787), hepatic damage (MESH:D056486), Liver Injury (MESH:D017093), inflammatory (MESH:D007249)
- **Chemicals:** GSH (MESH:D005978), APAP (MESH:D000082), Bioflavonoid (MESH:D005419), Saline (MESH:D012965), MDA (MESH:D015104), Tamarixetin (MESH:C508967)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12294041/full.md

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Source: https://tomesphere.com/paper/PMC12294041